Vitamin D deficiency rickets

Introduction to vitamin D deficiency rickets Vitamin D deficiency rickets (vitaminDdeficiencyrickets), which is a common disease in children, accounting for more than 95% of total rickets, this disease is due to insufficient vitamin D in the body caused by systemic calcium, phosphorus metabolism is abnormal, so that calcium salts can not normally sink in the growth of bones Partly, skeletal deformities eventually occur. Although the diagnosis of rickets is rarely directly life-threatening, it is easy to be neglected due to slow onset. Once the obvious symptoms occur, the body's resistance is low, and it is easy to have pneumonia, diarrhea, anemia and other diseases. basic knowledge Sickness ratio: 0.05% Susceptible people: children Mode of infection: non-infectious Complications: anemia, chicken breast, funnel chest

Causes of vitamin D deficiency rickets

Insufficient sunshine (18%):

7-dehydrocholesterol in the skin needs to be converted to vitamin D 3 by ultraviolet radiation with a wavelength of 296-310 nm. Because ultraviolet rays cannot pass through the glass window, the lack of outdoor activities in infants and young children leads to insufficient production of endogenous vitamin D. Medium and high buildings can block sunlight, and atmospheric pollution such as smoke and dust will also absorb some ultraviolet rays. In winter, the sun is short and the ultraviolet rays are weak, which is likely to cause vitamin D deficiency.

Insufficient intake (20%):

Natural foods contain less vitamin D, which can't meet the needs. The amount of raw material D in milk is very small. Although the proportion of calcium and phosphorus in human milk is suitable (2:1), it is beneficial to the absorption of calcium. However, if breastfeeding children lack outdoor Activities, or not timely supplemented with cod liver oil, egg sway, liver mud and other food supplements rich in vitamin D, are also prone to rickets.

Overspeed (14%):

Vitamin D stored in premature or twin-baby infants is insufficient, and the growth rate after birth is fast, requiring more vitamin D. It is prone to vitamin D deficiency rickets. Infants with slow growth have fewer fistulas.

Disease factor (10%):

Most gastrointestinal or hepatobiliary diseases can affect the absorption of vitamin D, such as infantile hepatitis syndrome, congenital biliary stricture or atresia, steatorrhea, pancreatitis, chronic diarrhea, etc.; severe liver and kidney damage can also cause vitamin D hydroxylation disorders The amount of production is insufficient to cause rickets.

Drug impact (8%):

Long-term use of anticonvulsant drugs can make vitamin D deficiency in the body, such as phenytoin, phenobarbital, etc. can increase the activity of hepatocyte microsomal oxidase system, accelerate the decomposition of vitamin D and 25 (OH) D into inactive metabolites Glucocorticoids fight the action of vitamin D to transport calcium.

Vitamin D deficiency rickets prevention

Special precautions for rickets

1. Promote breastfeeding and add vitamin D and calcium in a timely manner.

Baby supplement foods with appropriate phosphorus ratio.

2, more sun, the average daily outdoor activity time should be more than one hour, and more exposed skin.

3, for the weak children or when the outdoor activities in the winter and spring season are restricted, vitamin D can be supplemented, 400-800 international units per day.

Vitamin D deficiency rickets complications Complications Anemia chicken chest funnel chest

1, the disease is mainly caused by the baby looking up, sitting, standing, walking later. The joints are loose and overextended, and the cerebral cortex is abnormally characterized by slow conditioned reflexes, backward language development, and anemia.

2, in some of the more serious rickets, there will be other bone deformation, such as chicken breasts, funnel chest, X-legs, O-legs, ribbed beads, bracelets and anklets.

Vitamin D deficiency rickets symptoms Common symptoms Scoliosis spine bending alopecia varus bone softening joint relaxation thoracic deformity night terror

The child with this disease may have the following symptoms:

(A) mental and neurological symptoms: sweating, night terrors, crying and so on. Excessive sweat has nothing to do with the climate. Because sweat is irritated, the child often rubs the occiput to form a bald or ring-shaped hair loss.

(2) Osteophyte performance.

1, the head.

(1) Skull softening: It is an early manifestation of rickets, which is more common in infants from March to June.

(2) Cranial deformity: "square skull", "saddle head" or "crosshead"

(3) The front is large, the closure is late, and it can be closed until 2-3 years old.

(4) Late teething can be extended to 1 year old teething, or 3 years old. In severe cases, the teeth are not aligned and the enamel is poorly developed.

2, chest.

(1) The ribs are affected by beads.

(2) Thoracic deformity: chicken chest; funnel chest.

3, limbs and spine.

(1) The wrist and ankle are inflated to form a bangle and a foot bracelet.

(2) Lower limb deformity "O" shaped leg (knee varus), or "X" shaped leg (knee valgus).

(3) curvature of the spine: there may be scoliosis or kyphosis. In severe cases, pelvic deformity (hip valgus) may also be seen. In severe cases, women may become dystocia due to pelvic deformity in adulthood.

(3) Other performances: heads up, sitting, standing, walking are late, joints are loose and overextended, cerebral cortex is abnormal, conditioned reflexes are slow, language development is backward, and anemia is observed.

Examination of vitamin D deficiency rickets

1. Laboratory inspection:

(1) Alkaline phosphatase increased earlier in the course of rickets, and recovered at the latest. It is good for checking the diagnosis.

(2) Determination of serum 25(OH)D3 or 1,25(OH)2D3 levels, the value of which is zero in typical rickets, and also significantly decreased in subclinical rickets, and vitamin D can be significantly increased after treatment, which is sensitive. Reliable biochemical indicators.

2, X-ray inspection:

X-ray changes were evident in long bones with faster bone development, especially at the distal end of the radius and the proximal humerus.

Diagnosis and identification of vitamin D deficiency rickets

The disease needs to be identified with the following diseases:

1. Renal rickets:

Kidney disease causes renal dysfunction to reduce the production of 1,25(OH) D, causing rickets, low blood calcium, and high blood phosphorus. It is necessary to use 1,25(OH) D for effective treatment.

2, hepatic rickets:

Various liver diseases lead to liver dysfunction, which can cause 1,25(OH) D production disorder; if accompanied by biliary obstruction, it will not only affect the absorption of vitamin D, but also inhibit the absorption of calcium due to the formation of calcium soap, resulting in low Blood calcium and rickets signs.

3, distal renal tubular acidosis:

The child is short, skeletal deformity, metabolic acidosis, polyuria, alkaline urine, in addition to low blood calcium and low blood phosphorus, often also low blood potassium.

4. Vitamin D-dependent rickets:

The disease is autosomal recessive and can be divided into two types. Type I is a defect of 1-hydroxylase in the kidney, type II is a defect in the target organ 1,25(OH) D receptor, clinical manifestations are severe rickets, blood calcium and phosphorus are significantly decreased, and alkaline phosphatase is significantly elevated. Secondary hyperparathyroidism. Type I children may have high amino aciduria, and type II children are characterized by alopecia.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.